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Old 02-19-2011
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Eye Glaucoma Concept.

Could someone please explain me Open angle and Close angle glaucoma - their pathologies and treatments please? I have tried understanding from Kaplan Pharm and FA but somehow i am not fully understanding it.

Any help will be appreciated.

Thanks in advance.
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Old 02-19-2011
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First, u need not worry about open-angle glaucoma. it is totally and totally silent. No symptoms until u lose eyesight. So, no clinical cases can be made from it and not tested. Thanks Conrad Fishy for telling me this; at least one thing less to worry about!

Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress at a slower rate and the patient may not notice that they have lost vision until the disease has progressed significantly.

The major risk factor for most glaucomas and focus of treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation. In open angle glaucoma there is reduced flow through the trabecular meshwork; in angle closure glaucoma, the iris is apposed to the lens resulting in the inability of the aqueous fluid to flow from the posterior to the anterior chamber and then out of the trebecular network.

Treatment Options:
Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow
Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.
Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous humor production and increasing trabecular outflow.
Less-selective sympathomimetics such as epinephrine decrease aqueous humor production through vasoconstriction of ciliary body blood vessels.
Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour. Ecothiopate is used in chronic glaucoma.
Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
Physostigmine is also used to treat glaucoma and delayed gastric emptying.
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The above post was thanked by:
Awwad (07-27-2013), donofitaly (02-20-2011), KB24 (04-14-2015), Rabin Basnet (08-05-2015), Sabio (02-19-2011), Taiwan_Guy (09-06-2011), tariqkaseda (10-25-2011), wimzie (02-21-2011)



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